This press release contains:
---Summaries of newsworthy papers:
Medicine: Vitamin E may be bad for bones
Neuroscience: Sensing sustained environmental threats
---Mention of papers to be published at the same time with the same embargo
---Geographical listing of authors
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[1] Medicine: Vitamin E may be bad for bones
DOI: 10.1038/nm.2659
Vitamin E decreases bone mass by stimulating the generation of bone-degrading cells, reports an article published online this week in Nature Medicine. As vitamin E containing supplements are widely consumed, these results may have public-health implications.
Bone strength is maintained by the balance between bone-forming cells, called osteoblasts, and bone-degrading cells, called osteoclasts, which are formed by the fusion of precursor cells. Although the role of fat-soluble vitamins such as vitamin D in maintaining bone strength is well known, the role of vitamin E, or alpha-tocopherol, is less clear. Early studies had shown a positive effect of vitamin E on bone. This effect was proposed to be dependent on the antioxidant properties of alpha-tocopherol.
By contrast, Shu Takeda and his colleagues report that mice deficient in an alpha-tocopherol transfer protein, a model of vitamin E deficiency, have high bone mass as a result of a decrease in bone degradation. The team found that alpha-tocopherol stimulated the fusion of osteoclast precursor cells, independently of its antioxidant capacity, by inducing the expression of a series of molecules crucial for osteoclast formation. Moreover, healthy mice or rats fed a diet with an amount of alpha-tocopherol similar to what is found in supplements consumed by many people lost bone mass, highlighting the potential relevance of these findings to human health.
Author contact:
Shu Takeda (Keio University, Tokyo, Japan)
Tel: +81 3 3353 1211; E-mail: [email protected]
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[2] Neuroscience: Sensing sustained environmental threats
DOI: 10.1038/nn.3061
The mechanisms that mediate the behavior of the worm C. elegans in response to environmental oxygen concentration are described in a study published online this week in Nature Neuroscience. These results represent an important step in our understanding of how animals implement persistent defense behaviors.
All organisms have to deal with a barrage of environmental information. Sensory systems have therefore evolved adaptive mechanisms that allow them to only react briefly to most stimuli, or rapidly ignore some of them. However, certain harmful stimuli have to hold our attention for a prolonged period of time, but the mechanisms that mediate this sustained response are not fully understood.
In the wild, C. elegans is likely exposed to oxygen concentrations varying from very low to very high levels. When exposed to higher or lower oxygen concentrations, the worm responds by changing speed or direction, or by aggregating with other worms to collectively reduce oxygen concentrations. Mario De Bono and colleagues studied the oxygen-sensing neurons of the worm, called ‘tonic’ sensors, that respond continuously during oxygen exposure. Using a set of genetic tools, the scientists worked out the molecular mechanisms in these neurons that are required to generate these tonic signals, and determined how these signals are transformed in different downstream neurons to elicit short and long-term behaviors.
Author contact:
Mario De Bono (MRC Laboratory of Molecular Biology, Cambridge, UK)
Tel: +44 1223 402278; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[3] Corticostriatal plasticity is necessary for learning intentional neuroprosthetic skills
DOI: 10.1038/nature10845
[4] Coevolution in multidimensional trait space favours escape from parasites and pathogens
DOI: 10.1038/nature10853
[5] Enzymatic catalysis of anti-Baldwin ring closure in polyether biosynthesis
DOI: 10.1038/nature10865
[6] Chromatin-modifying enzymes as modulators of reprogramming
DOI: 10.1038/nature10953
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[7] CDK5 and MEKK1 mediate pro-apoptotic signalling following endoplasmic reticulum stress in an autosomal dominant retinitis pigmentosa model
DOI: 10.1038/ncb2447
[8] A size-exclusion permeability barrier and nucleoporins characterize a ciliary pore complex that regulates transport into cilia
DOI: 10.1038/ncb2450
[9] Homeostatic control of recombination is implemented progressively in mouse meiosis
DOI: 10.1038/ncb2451
[10] Lrig1 controls intestinal stem-cell homeostasis by negative regulation of ErbB signaling
DOI: 10.1038/ncb2464
[11] Fbxw7a- and GSK3-mediated degradation of p100 is a pro-survival mechanism in multiple myeloma
DOI: 10.1038/ncb2463
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[12] Peptides induce persistent signaling from endosomes by a nutrient transceptor
DOI: 10.1038/nchembio.910
NATURE CHEMISTRY (http://www.nature.com/nchem)
[13] Self-assembly of the oxy-tyrosinase core and the fundamental components of phenolic hydroxylation
DOI:10.1038/nchem.1284
[14] Metal-directed, chemically tunable assembly of one-, two- and three-dimensional crystalline protein arrays
DOI:10.1038/nchem.1290
NATURE CLIMATE CHANGE (http://www.nature.com/nclimate)
[15] Climate response to zeroed emissions of greenhouse gases and aerosols
DOI: 10.1038/nclimate1424
[16] Reconciling top-down and bottom-up modelling on future bioenergy deployment
DOI: 10.1038/nclimate1416
[17] Trade-offs and synergies in urban climate policies
DOI: 10.1038/nclimate1434
[18] Black-carbon reduction of snow albedo
DOI: 10.1038/nclimate1433
Living in the doughnut
DOI: 10.1038/nclimate1457
NATURE GENETICS (http://www.nature.com/naturegenetics)
[19] Mutations in axonemal dynein assembly factor DNAAF3 cause primary ciliary dyskinesia
DOI: 10.1038/ng.1106
[20] A new subtype of bone sarcoma defined by BCOR-CCNB3 gene fusion
DOI: 10.1038/ng.1107
[21] A genome-wide association study identifies two susceptibility loci for duodenal ulcer in the Japanese population
DOI: 10.1038/ng.1109
[22] Ascorbic acid prevents loss of Dlk1-Dio3 imprinting and facilitates generation of all-iPS cell mice from terminally differentiated B cells
DOI: 10.1038/ng.1110
[23] Complex reorganization and predominant non-homologous repair following chromosomal breakage in karyotypically balanced germline rearrangements and transgenic integration
DOI: 10.1038/ng.2202
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[24] NF-kappaB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance
DOI:10.1038/ni.2238
[25] NLRP4 negatively regulates type I interferon signaling by targeting the kinase TBK1 for degradation via the ubiquitin ligase DTX4
DOI:10.1038/ni.2239
NATURE MATERIALS (http://www.nature.com/naturematerials)
[26] On the molecular origin of supercapacitance in nanoporous carbon electrodes
DOI: 10.1038/nmat3260
Nature MEDICINE (http://www.nature.com/naturemedicine)
[27] Tyrosine phosphatase SHP2 promotes breast cancer progression and maintains tumor-initiating cells via activation of key transcription factors and a positive feedback signaling loop
DOI: 10.1038/nm.2645
[28] Macrophage-derived Wnt opposes Notch signaling to specify hepatic progenitor cell fate in chronic liver disease
DOI: 10.1038/nm.2667
[29] IL-17A produced by alpha-beta T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction
DOI: 10.1038/nm.2684
NATURE METHODS (http://www.nature.com/nmeth)
[30] Long-term, efficient inhibition of microRNA function in mice using rAAV vectors
DOI: 10.1038/nmeth.1903
[31] TULIPs: Tunable, light-controlled interacting protein tags for cell biology
DOI: 10.1038/nmeth.1904
[32] Fast gapped read alignment with Bowtie 2
DOI: 10.1038/nmeth.1923
[33] Computerized video analysis of social interactions in mice
DOI: 10.1038/nmeth.1924
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[34] The growth factor SVH-1 regulates axon regeneration in C. elegans via the JNK MAPK cascade
DOI: 10.1038/nn.3052
[35] Mitochondrial CB1 receptors regulate neuronal energy metabolism
DOI: 10.1038/nn.3053
[36] The voltage-gated proton channel, Hv1, enhances brain damage from ischemic stroke
DOI: 10.1038/nn.3059
[37] Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons
DOI: 10.1038/nn.3060
NATURE PHOTONICS (http://www.nature.com/nphoton)
[38] Frequency comb generation at terahertz frequencies by coherent phonon excitation in silicon
DOI: 10.1038/nphoton.2012.35
[39] A comparison of graphene, superconductors and metals as conductors for metamaterials and plasmonics
DOI: 10.1038/nphoton.2012.27
[40] Heralded quantum entanglement between two crystals
DOI: 10.1038/nphoton.2012.34
Nature PHYSICS (http://www.nature.com/naturephysics)
[41] Three-dimensional localization of ultracold atoms in an optical disordered potential
DOI: 10.1038/nphys2256
[42] Nodal superconducting-gap structure in ferropnictide superconductor BaFe2(As0.7P0.3)2
DOI: 10.1038/nphys2248
[43] Satellites and large doping and temperature dependence of electronic properties in hole-doped BaFe2As2
DOI: 10.1038/nphys2250
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[44] The structure of the ASAP core complex reveals the existence of a Pinin-containing PSAP complex
DOI: 10.1038/nsmb.2242
[45] The SUMO protease SENP7 is a critical component to ensure HP1 enrichment at pericentric heterochromatin
DOI: 10.1038/nsmb.2244
[46] Structure of the human metapneumovirus fusion protein with neutralizing antibody identifies a pneumovirus antigenic site
DOI: 10.1038/nsmb.2250
[47] A sensor-adaptor mechanism for enterovirus uncoating from structures of EV71
DOI: 10.1038/nsmb.2255
[48] Topoisomerase I poisoning results in PARP-mediated replication fork reversal
DOI: 10.1038/nsmb.2258
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GEOGRAPHICAL LISTING OF AUTHORS
The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.
AUSTRALIA
Roseworthy: 23
Sydney: 35
AUSTRIA
Klosterneuburg: 37
Vienna: 30
BELGIUM
Leuven: 12, 28
CANADA:
Burnaby: 15
Montreal: 15
Quebec: 23
CHINA
Beijing: 30, 47
Chengdu: 30
Nanjing: 25
Shanghai: 42
FRANCE
Bordeaux: 20, 35
Orsay: 33
Palaiseau: 43
Paris: 17, 20, 26, 33, 41, 43, 44, 45
Talence: 41
Toulouse: 17
Tours: 2, 26
GERMANY
Berlin: 16
Heidelberg: 4
Mainz: 35
Martinsried: 44
Munster: 19
Postdam: 16
GREECE
Crete: 39
ISRAEL
Tel-Aviv: 19
ITALY
Milan: 27, 48
Rome: 35
JAPAN
Aichi: 21
Chiba: 43
Ibaraki: 43
Kanagawa: 21
Nagoya: 34
Osaka: 1, 10
Saitama: 43
Sapporo: 5
Shizuoka: 5
Tokyo: 1, 19, 21, 38, 43
Tsukuba: 34, 38
Yokohama: 29
NETHERLANDS
Amsterdam: 28
Utrecht: 10, 28
NEW ZEALAND
Auckland: 23
PORTUGAL
Lisbon: 3
SINGAPORE
Singapore: 5
SPAIN
Barcelona: 9
Leioia: 35
Madrid: 35
Salamanca: 48
Seville: 10
SAUDI ARABIA
Jeddah: 19
SWEDEN
Lund: 43
SWITZERLAND
Basel: 27
Bern: 35
Fribourg: 43
Geneva: 40
Zurich: 43, 48
TAIWAN
Taichung: 4
TURKEY
Ankara: 4
UNITED KINGDOM
Cambridge: 2, 10
Didcot: 47
Edinburgh: 28
Faversham: 2
Glasgow: 28
Hertfordshire: 48
Leeds: 47
Leicester: 19
London: 10, 19, 22
Oxford: 5, 24, 26, 47
UNITED STATES OF AMERICA
California
Berkeley: 3, 18
Chico: 13
La Jolla: 11, 14, 48
Los Angeles: 5
Menlo Park: 5
Richmond: 16
San Francisco: 29
Stanford: 13, 45
District of Columbia
Washington: 17
Idaho
Moscow: 4
Illinois
Chicago: 31
Evanston: 31, 46
Iowa
Ames: 39
Kansas
Pittsburgh: 38
Maryland
Baltimore: 32
Bethesda: 3
Chevy Chase: 4
College Park: 32
Massachusetts
Boston: 4, 22, 23, 27, 30, 36
Cambridge: 4, 22, 23
Worcester: 30
Michigan
Ann Arbor: 8, 11
Minnesota
Minneapolis: 24
New York
New York: 7, 9, 11, 19, 22, 43
Tarrytown: 11
North Carolina
Research Triangle Park: 27
Pennsylvania
Philadelphia: 26
Tennessee
Knoxville: 4
Nashville: 46
Texas
Houston: 25
Utah
Salt Lake City: 34
Virginia
Charlottesville: 23
Fairfax: 14
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Nature Materials (London)
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Nature Medicine (New York)
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Nature Methods (New York)
Hugh Ash
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Nature Nanotechnology (London)
Peter Rodgers
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Nature Neuroscience (New York)
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Tel: +1 212 726 9319; E-mail: [email protected]
Nature Photonics (Tokyo)
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Tel: +81 3 3267 8776; E-mail: [email protected]
Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]
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